Murine models: γδ T cells in AT and adiposity
Study | IL-17+ γδ T cells | IFNγ+ γδ T cells | Number/functions | Reference |
---|---|---|---|---|
γδ T cells in AT | Present | Inhibition of adipogenesis | [31] | |
γδ T cells in AT | Present | Induction of IL-33 production; γδ T cells are responsible for non-shivering thermogenesis | [32] | |
γδ T cells in AT | Present | Binds to the IL-17RC, increases sympathetic innervation | [33] | |
γδ T cells in AT, effect of KD | Short term KD increases anti-inflammatory γδ T cells, long term-induces obesity and depletes γδ T cells in AT | [34] | ||
IEL γδ T cells | Express GLP-1R, forming a “depleting sink” for GLP-1R, thus possibly contributing to obesity | [35] | ||
γδ T cells in AT-effect of HFD induced obesity | HFD increased γδ T cells in inguinal fat | [36] | ||
γδ T cells in AT-effect of HFD induced obesity | HFD increased γδ T cells. AT was decreased in the absence of leptin | [37] | ||
γδ T cells in AT-effect of HFD in TL1A deficient mice | TL1A deficient mice were less obese and had fewer γδ T cells in AT | [38] | ||
Subsets of γδ T cells in AT, effect of HFD | Present, mainly Vγ4 and 6+ | HFD induces an increase of CD44+CD62lo γδ T cells in epididymal fat which appear to play a proinflammatory role | [39] | |
Effect of a transgene PPAR-β expressed in T cells on HFD and IR | Mice bearing Tg T-PPAR-β in T cells have depleted αβ T cells and no change in γδ T cell number resulting in an increased γδ/αβ T cell ratio in lymphoid organs and preserved γδ T cells in WAT. These mice have less IR and are less obese | [40] | ||
Hyperglycemic obese mice | Reduced skin γδ cells dysfunctional in keratinocyte repair | [42–44] | ||
Effect of HFD on imiquimod induced psoriasis | More γδ low cells expressing PD1 in the skin | [45] | ||
Obesity-related to adiponectin deficiency in psoriasis | Elevated in the skin by obesity | Reduced by adiponectin | [46] | |
Effect of HFD on Corynebacterium activated skin γδ T cells | Elevated in the skin by HFD | [47] | ||
Effect of obesity on ozone induces lung changes | Increase of IL-13+ and ST2 related IL-33 responsive γδ T cells in the lung | [48] | ||
Effect of obesity on γδ T cells in the lung | Elevated by HFD in the lung | Increased airway hyperresponsiveness | [49] | |
Effect of HFD on gut T cells | IEL, which express GLP-1R, CD69, and CD103 are decreased by HFD, leading to increased sensitivity to dextran sulfate-induced colitis | [50–52] | ||
Deficiency of integrin β7-effect on HFD | Decreased GLP-1R+ γδ and αβ IEL, leading to resistance to HFD causing obesity, due to decrease of GLP-1R | [35] | ||
Effect of obesity on ocular T cells in NRF2–/– mice (model for AMD) | Increased in the eye | Induction of retinal lesions | [53] | |
A high cholesterol diet in mice | Reduced number of γδ T cells in the thymus, colonic submucosa, and early tumorogenesis | [54] | ||
Effect of 27-hydroxycholesterol | An increase in the number of polymorphonuclear neutrophils and pro tumoral γδ T cells at distal metastatic sites | [55] | ||
Diet-induced obesity | CCR6+ pro-tumoral γδ T cells attracted to chemically induced colon adenocarcinoma | [56] | ||
Metabolic characteristics of pro and anti-tumoral γδ T cells and effect of the obesity | IL-17 producing cells are dependent upon oxidative phosphorylation, exhibit high lipid uptake and increase in obesity | IFNγ producing γδ T cells are dependent upon glycolysis | IL-17+ γδ T cells were pro-tumoral, whereas IFNγ+ cells were anti-tumoral | [57] |
GLP-1R: glucagon-like peptide-1 receptor; PD1: programmed death 1; NRF2: nuclear erythroid 2-related factor 2; AMD: age-related macular degeneration; CCR6: C-C motif chemokine receptor 6